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Systemic Analysis of Atg5-Null Mice Rescued from Neonatal Lethality by Transgenic ATG5 Expression in Neurons.
https://repo.qst.go.jp/records/48184
https://repo.qst.go.jp/records/48184061616e8-57ea-4290-bebe-796a4012e7df
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-07-25 | |||||
タイトル | ||||||
タイトル | Systemic Analysis of Atg5-Null Mice Rescued from Neonatal Lethality by Transgenic ATG5 Expression in Neurons. | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
R, Yoshii Saori
× R, Yoshii Saori× Kuma, Akiko× Akashi, Takumi× Hara, Taichi× Yamamoto, Atsushi× Kurikawa, Yoshitaka× Itakura, Eisuke× Tsukamoto, Satoshi× Shitara, Hiroshi× Eishi, Yoshinobu× Mizushima, Noboru× 塚本 智史 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Autophagy is a cytoplasmic degradation system that is important for starvation adaptation and cellular quality control. Previously, we reported that Atg5-null mice are neonatal lethal; however, the exact cause of their death remains unknown. Here, we show that restoration of ATG5 in the brain is sufficient to rescue Atg5-null mice from neonatal lethality. This suggests that neuronal dysfunction, including suckling failure, is the primary cause of the death of Atg5-null neonates, which would further be accelerated by nutrient insufficiency due to a systemic failure in autophagy. The rescued Atg5-null mouse model, as a resource, allows us to investigate the physiological roles of autophagy in the whole body after the neonatal period. These rescued mice demonstrate previously unappreciated abnormalities such as hypogonadism and iron-deficiency anemia. These observations provide new insights into the physiological roles of the autophagy factor ATG5. | |||||
書誌情報 |
Developmental cell 巻 39, 号 1, p. 116-130, 発行日 2016-10 |
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出版者 | ||||||
出版者 | Cell Press | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1534-5807 | |||||
PubMed番号 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | 27693508 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.devcel.2016.09.001 |